Recent computational investigations have shed light into the various hydrodynamic mechanisms at play during arterial gas embolism that may result in endothelial cell (EC) injury. Other recent studies have suggested that variations in hematocrit level may play an important role in determining the severity of neurological complications due to decompression sickness associated with gas embolism.To develop a comprehensive picture, we computationally modeled the effect of hematocrit variations on the motion of a nearly occluding gas bubble in arterial blood vessels of various sizes. The computational methodology is based on an axisymmetric finite difference immersed boundary numerical method to precisely track the blood-bubble dynamics of the interface. Hematocrit variations are taken to be in the range of 0.2-0.6. The chosen blood vessel sizes correspond to small arteries and small and large arterioles in normal humans.Relevant hydrodynamic interactions between the gas bubble and EC-lined vessel lumen have been characterized and quantified as a function of hematocrit levels. In particular, the variations in shear stress, spatial and temporal shear stress gradients, and the gap between bubble and vascular endothelium surfaces that contribute to EC injury have been computed.The results suggest that in small arteries, the deleterious hydrodynamic effects of the gas embolism on an EC-lined cell wall are significantly amplified as the hematocrit levels increase. However, such pronounced variations with hematocrit levels are not observed in the arterioles.